One way for a cell to become cancerous is to prevent the shortening of its telomeres, the repetitive DNA sequences at the ends of chromosomes that normally decrease in length each time the cell divides, leading to senescence and death. Aylin Rizki and Victoria Lundblad of Baylor College of Medicine, Houston, Texas, have found that, in yeast, this can happen because of a breakdown in the cell's DNA-proofreading machinery (Nature, Vol. 411, No. 6838, 07 Jun 2001).

The researchers looked at yeast strains lacking the genes that normally prevent errors in DNA copying and exchange between chromosomes. These cells could survive indefinitely by swapping non-matching sequences of DNA, thereby maintaining the length of their telomeres. This may be another mechanism by which human cells proliferate, in addition to the reactivation of telomerase (the telomere-building enzyme). It may also have implications for anti-cancer drugs aimed solely at telomerase.

In an accompanying News and Views article, Raju Kucherlapati of the Albert Einstein college of Medicine, New York, and Ronald DePinho of the Harvard Medical School, Boston, describe the research as "a prime example of how studies of yeast guide our understanding of complex human diseases".

Social bookmarking allows users to save and categorise a personal collection of bookmarks and share them with others. This is different to using your own browser bookmarks which are available using the menus within your web browser.

Use the links below to share this article on the social bookmarking site of your choice.